Several aspects of the interaction of the complement system with Actinomyces viscosus T14V, an organism implicated in the pathogenesis of periodontal disease, are under exploration. Complement fixation by monoclonal antibodies is being used to localize epitopes on the fimbriae of these bacteria and associate them with functional properties of the fimbriae. Antibodies with different specificities for the type 1 fimbriae (which mediate attachment to saliva treated hydroxyapatite) have been found to cooperate in activation of complement. Three patterns of complement fixation have been identified: additive responses by antibodies which react with the same epitope, inhibition of complement fixing antibodies by non-complement fixing antibodies reacting with the same epitope and synergistic responses by antibodies reacting with different epitopes. Studies utilizing the F(ab')2 fragments of these antibodies indicate that the Fc portions of each of two antibodies must participate in additive or synergistic responses. Inflammatory consequences of complement activation may be attributable, in part, to complement mediated stimulation of macrophages resulting in their production of prostaglandins. Thus, cultures of macrophages incubated with antibodies to their surface antigens and complement produce prostaglandin E. This effect requires the late acting complement components and can be significantly potentiated by the exogenous addition of the prostaglandin precursor, arachidonic acid.